Although the liver is not considered to be a primary target of testosterone action, androgens maintain specific male pattern of pituitary GH secretion and actions on liver [78], and it has been shown that specific deletion of androgen receptor (AR) in liver of male animals causes hepatic insulin resistance with decreased fatty acid β-oxidation and steatosis [79], which implicates the hepatic AR as a positive factor in maintaining physiological control of glucose and lipid homeostasis. This evidence concerns the gene INS and steatosis.